Moriel H. Vandsburger1, Brent A. French1,2, Christopher M. Kramer2,3, Frederick H. Epstein1,2
1Biomedical Engineering, University of Virginia, Charlottesville, VA, USA; 2Radiology, University of Virginia, Charlottesville, VA, USA; 3Medicine, University of Virginia, Charlottesville, VA, USA
Modulation of L-Type Calcium Channel (LTCC) flux plays an important role in calcium cycling and cardiomyocyte contractility. Manganese (Mn2+) enters cardiomyocytes through the LTCC and shorterns T1 proportionatly. Modulation of LTCC flux by neuronal (nNOS) and endothelial (eNOS) isoforms of nitric oxide synthase is unclear. The uptake of Mn2+ was examined in wild type (WT), nNOS-/-, and eNOS-/- mice at baseline and with dobutamine using an ECG-gated saturation recovery pulse sequence with constant repetition time (TR) of 200ms. Whereas baseline LTCC flux was higher in nNOS-/- mice and unchanged with dobutamine, LTCCI increased with dobutamine in WT and eNOS-/- mice.